肺癌患者亲属对癌症具有易感性的研究

分析了３７０例肺癌先证者的核心家系和３０个对照的核心家系资料，发现肺癌先证者的亲属（父母，同胞）患癌症的危险性明显高于对照的亲属（父母，同胞）前者是后者的２．０７倍（Ｐ〈０．０１）。其中患肺癌的危险性是亲属的１．８５倍，患其它癌症的危险性是３．７８倍，差别均具有高度显著性统计学意义，表明了宣城威肺癌患者的亲属不仅对肺癌的易感性增高，而且对其它癌症的易感性也较高，这些结果都支持了肺癌患者的家系亲属对     

肺癌患者亲属对癌症有易感性的研究

分析了３７０例肺癌先证者的核心家系和３７０个对照的核心家系资料，发现肺癌先证者的亲属（父母、同胞）患癌症的危险性明显高于对照的亲属（父母、同胞），前乾是后者的２．０７倍（Ｐ〈０．０１）。其中患癌的危险性是对照亲属的１．８５倍，患其它癌症的危险性是３．７８倍，差别均具有高度显著性统计学意义，表明了宣威肺癌患者的亲属不仅对肺癌的易感性增高，而且对其它癌症的易感性也较高。这些结果都支持了肺癌患者的家系亲属对癌症具有遗传易感性的假设。     

女性肺癌的遗传流行病学研究

通过对１７６个女性肺癌先证者核心家系和１９４个女性对照的核心家系资料分析。发现女性肺癌先证者的一级亲属（父母、同胞）患肺癌的危险性是对照一级亲属（父母、同胞）的１．６７倍，且差异具有显著性。其中女性亲属患肺癌的危险性显著高于对照的女性亲属，ＯＲ值为２．８１（Ｐ＜０．０１）。女性肺癌的遗传度为２０．５４％，遗传因素是女性肺癌的重要危险因素。女性肺癌先证者的女性亲属对肺癌的遗传易感性比男性亲属高。这些结果有助于全面阐明云南省宣威县女性肺癌高发的原因。     

男性肺癌的遗传流行病学研究

为深入研究宣威县男性肺癌的病因，探讨遗传因素的作用，分析了１９４例男性肺癌先证者的核心家系和１７６例男性对照的核心家系资料。结果发现，肺癌先证者的亲属（父母、同胞）患肺癌的危险性是对照组的１．７８倍，且差异有显著性。其中，父母及女性亲属患肺癌的危险性分别是对照组的２．９０倍和２．４３倍，差异均有显著性意义。肺癌的遗传度为２４．６８％。女性对肺癌的遗传易患性比男性高，遗传因素是肺癌的重要危险因素。     

2型糖尿病核心家系的遗传易感性研究

通过对２型糖尿病（ＮＩＤＤＭ）核心家系的分析,探讨了遗传因素在核心家系成员中所起作用的程度。结果表明：病例核心家系一级亲属ＮＩＤＤＭ 的发病率非常显著的高于对照组,χ２ ＝ １７．０,Ｐ＜ ０．００１,相对危险度（ＲＲ）为３．３０,９５％ 可信区间为１．８０～６．０５。不论父母、同胞和子女,均以病例亲属的发病率显著高于对照;病例组各亲属中,不论男女和年龄,标准化发病率比（ＳＩＲ）均明显高于对照人群的１００,经统计学Ｚ检验有极显著意义;病例核心家系的ＲＲ、归因危险度（ＡＲ）％ 也明显较高,进一步说明血缘关系与ＮＩＤＤＭ 之间有较强的联系。     

脑梗塞家族聚集性的病因和流行病学研究

本研究通过遗传流行病学病例对照方法，对宜兴市２１４个家系（１０９个脑梗塞先证家系和１０５个对照家系）进行了脑梗塞家族史的遗传易感性研究，结果表明：病例和对照家系有良好的均衡可比性，病例组一级亲属总的患病率为５．１２％，与对照组的１．６３％相比，差异有非常显著性，不论其父母或同胞，均以病例亲属的患病率显著高于对照，而子女中两者无显著性差异；二项分布显示，脑梗塞家族中实际发病数超过其二项分布的理论概率     

宣威肺癌的遗传流行病学研究

分析了宣威肺癌高发区的３７０对核心家系的资料。结果表明；肺癌的发生具有家族聚集性，肺癌先证者的亲属患肺癌的危险性增加，是配偶家系亲属的１．８５倍。女性亲属是配偶家系女性亲属的２．６４倍。肺癌的遗传属于多基因遗传，其分离比为０．１５，其遗传度为２４．６％，肺癌先证者的亲属对肺癌的易感性比配偶的亲属高。遗传因素是肺癌的危险因素，但不是宣威肺癌高发的主要危险因素。     

慢性阻塞性肺部疾病的家族聚集性分析

为了判断慢性阻塞性肺部疾病（ＣＯＰＤ）的家族聚集性，探讨遗传因素对ＣＯＰＤ发病的影响，分析了２０６对核心家系的资料。结果表明：ＣＯＰＤ的发病具有家族聚集性。ＣＯＰＤ先证者的亲属（父母、兄弟姐妹）患ＣＯＰＤ的危险性增加，是对照家系亲属（父母、兄弟姐妹）的２．０７倍。除母亲之外，两家系父亲间，兄弟间及姐妹间患ＣＯＰＤ危险性的差异均具有显著性。故ＣＯＰＤ先证者的亲属对ＣＯＰＤ的易感性比对照的亲属高，说明遗传因素是ＣＯＰＤ的危险因素之一。     

脑梗塞遗传病因的流行病学系列研究(Ⅰ)

通过遗传流行病学病例对照方法，对宜兴市２１４个家系（１０９个脑梗塞先证家系和１０５个对照家系）进行分离比、多基因遗传方式和遗传度的分析。结果表明：在病例和对照家系具有良好均衡可比性的前提下，脑梗塞的分离比为０．０５２９，显著低于０．２５，说明其不符合单基因遗传病的特征；多基因遗传方式的分析表明，其一级亲属的理论发病率为６．６７８％，与实际发病率８．６１１％相比，无统计学显著性差异，符合多基因遗传的特征；遗传度的估算显示；脑梗塞先证者的一级亲属中，遗传度为５３％，其中女性亲属的遗传度达５７％，显著高于男性亲属的３９．４％，说明在脑梗塞病因中，遗传因素起着一定的作用，特别是对女性作用更明显     

脑梗塞遗传病因的流行病学系列研究Ⅱ——核心家系的遗传易感 …

本研究通过对脑梗塞核心家系的分析，探讨了遗传因素在核心家系成员中所起作用的程度，结果表明，病例核心家系梗塞家族史的比例显著高于对照，ｘ＾２＝１８．４１，Ｐ〈０．００１，不同血缘亲属均有不同程度的脑梗塞患病率，从０．９３％到１２．８４％，病例组各亲属中，不论男女和年龄，ＳＭＲ均明显高于正常人群的１００，经统计学Ｚ检验有极显著意义，病例核心家系的ＲＲＡＲ、和调整率也明显较高，进一步说明血缘关系与脑梗塞     

Familial aggregation of breast cancer with early onset lung cancer.

Site-specific familial aggregation and evidence supporting Mendelian codominant inheritance have been shown in lung cancer. In characterizing lung cancer families, a number of other cancers have been observed. The current study evaluates whether first-degree relatives of early onset lung cancer cases are at increased risk of breast cancer. Families were identified through population-based lung cancer cases and controls under 40 years of age. Cases were ascertained through the Metropolitan Detroit SEER registry; controls through random-digit dialing. Data were available for 384 female relatives of 118 cases and 465 female relatives of 161 controls. Breast cancer in relatives was evaluated after adjusting for age, race, sex, and smoking status of each family member and the sex and age of the probands. A positive family history of early onset lung cancer increased breast cancer risk among first-degree relatives 5. 1-fold (95% CI, 1.7-15.1). Relatives of cases with adenocarcinoma of the lung were at highest risk (RR = 6.3, 95% CI 2.0-20). Mean age of breast cancer diagnosis among relatives of cases was 52.2 years and not statistically different from relatives of controls. Three case families also reported early ovarian cancers (mean age of diagnosis of 35 years). These findings suggest that shared susceptibility genes may act to increase risk of early onset lung and breast cancer in families.     

Genetic analysis of families with nonsmoking lung cancer probands

As part of a genetic epidemiologic study of lung cancer among nonsmokers, we investigated the role of genetic predisposition in familial aggregation. Cases were identified from the Metropolitan Detroit Cancer Surveillance System. Information on lung cancer occurrence, smoking habits (active or passive), and chronic respiratory diseases in first-degree relatives was obtained for 257 nonsmoking lung cancer probands (71 males, 186 females) diagnosed at ages 40–84 years. Among the 2,021 first-degree relatives, 24 (2.6%) males and 10 (1.1%) females were reported as having lung cancer. The occurrence of lung cancer among smoking and nonsmoking relatives was 4.5% and 1.1% in males and 2.8% and 0.4% in females, respectively. To evaluate the role of a putative Mendelian gene (one locus, two alleles) in the presence of other risk factors, we performed complex segregation analyses on the data using two different regressive model approaches [Segregation Analysis of a Discrete Trait Under a Class A Regressive Logistic Model, V4.0 (REGD) and Segregation Analysis of a Truncated Trait, V2.0, Model I (REGTL)] as implemented in the Statistical Analysis for Genetic Epidemiology (SAGE) program. Using either approach, an environmental model best explained the observed lung cancer aggregation in families ascertained through nonsmoking probands. Based on our final model, only 0.04% of this population had a very high risk and 4.2% had a moderate risk of lung cancer. The rest of the population had virtually no risk of lung cancer during their lifetime unless they have multiple risk factors. Among the high-risk individuals without any risk factor under study, the estimated risks at ages 40,60, and 80 years in males were 16.7%, 83.6%, and 95.4%, and in females were 14.0%, 72.2%, and 88.0%, respectively. Among at-moderate-risk smokers the estimated risks at the same age and gender groups were essentially the same as in the high-risk nonsmokers. Our results suggest that the pattern of lung cancer occurrence in families of nonsmoking lung cancer patients differs from that in families of smoking lung cancer patients. Despite the profound effect of smoking on the risk of lung cancer, other environmental and/or genetic risk factors need to be identified. Genet. Epidemiol. 14:181–197,1997. © 1997 Wiley-Liss, Inc.     

Increased familial risk for non-lung cancer among relatives of lung cancer patients

Reports of two or more anatomically distinct cancer types clustering in families suggest the possible existence of a susceptibility-to-cancer gene. To determine whether a genetic predisposition accounts for such familial aggregation, a retrospective case-control study was conducted in 1976-1979 of 337 southern Louisiana families in each of which a deceased lung cancer patient was used as the proband. A comparison of first-degree relatives of proband families with spouse (control) families revealed a significantly greater overall risk of cancer (odds ratio (OR) = 2.0, p less than 0.0001) in the proband group. Using logistic regression techniques to control for the confounding effects of age, sex, cigarette smoking, and occupational/industrial exposures, relatives of lung cancer probands maintained an increased risk of non-lung cancer (p less than 0.05). The crude odds ratio of a proband family having one family member with cancer was 1.67 compared with control families. Proband families were 2.16 times more likely to have two other family members with cancer. For three cancers and four or more cancers, the risk increased to 3.66 and 5.04, respectively. Each risk estimate was significant at the 0.01 level. The most striking differences in cancer prevalence between proband and control families were noted for cancer of the nasal cavity/sinus, mid-ear, and larynx (OR = 4.6); trachea, bronchus and lung (OR = 3.0); skin (OR = 2.8); and uterus, placenta, ovary, and other female organs (OR = 2.1). These data support the hypothesis of a genetic susceptibility to cancer in families with lung cancer.     

Familial risk of cancer among randomly selected cancer probands

Several investigators have reported that relatives of lung cancer probands have a greater-than-normal likelihood for developing some form of cancer. To evaluate whether this familial risk is general for probands with cancer at any site or limited to lung cancer probands, we did a case-control study in which probands having cancer affecting any body site were identified and their pedigree data were tabulated. Telephone interviews and a mailed questionnaire were used to obtain cancer histories and environmental exposures on the families of 41 lung cancer probands, 105 probands with cancer other than lung, and 127 spouse families. Cumulative tobacco exposure (P less than .05), occupational hazards (P less than .005), and age of the family relatives (P less than .0001) were found to be statistically significant predictors of cancer risk. With consideration given for these variables, we determined that siblings of lung cancer probands were at slightly greater risk of cancer of any kind (odds ratio [OR] = 1.43, P = .06) than siblings in the control group. Much of the elevated risk was attributable to an excess of lung cancer (OR = 2.49, P = .06). Siblings of non-lung/non-breast cancer probands were also determined to be at increased risk of lung cancer as well (OR = 1.61, P = .06). For parents, the risk was lower, although parental information may have been underreported.     

Increased cancer risk among relatives of nonsmoking lung cancer cases

Lung cancer has been shown to aggregate in families of nonsmoking lung cancer cases with an earlier age at onset. The current study evaluates whether relatives of nonsmoking lung cancer cases are at increased risk of cancers at sites other than lung. Families were identified through 257 population‐based, nonsmoking lung cancer cases and 277 population‐based, nonsmoking controls residing in metropolitan Detroit. Data were collected for 2,252 relatives of cases and 2,408 relatives of controls. First‐degree relatives of nonsmoking lung cancer cases were at 1.52‐fold (95% CI, 1.02–2.27) increased risk of cancer of the digestive system after adjustment for each relative's age, race, sex, and smoking status. Relative risk estimates also were elevated, but not significantly, for tobacco‐related cancers (RR = 1.39) and breast cancer (RR = 1.72). Among first‐degree relatives of younger probands (age 40–59), risk was non‐significantly increased 72% (95% CI 0.95–3.10) for all cancers combined and 3.14‐fold for cancers of the digestive system (95% CI 0.76–12.9). Nonsmoking relatives of cases were at increased risk of all cancer sites combined (RR = 1.32; 95% CI 1.003–1.73), cancers other than lung (RR = 1.37; 95% CI 1.03–1.82), and digestive system cancers (RR = 2.01; 95% CI 1.20–3.37). These findings of moderate familial aggregation for cancers of the lung, digestive system, breast, and tobacco‐related sites suggest that common susceptibility genes may act to increase risk for a variety of cancers in families. Genet. Epidemiol. 17:1–15, 1999. © 1999 Wiley‐Liss, Inc.     

Heterogeneity of breast cancer risk in families of young breast cancer patients and controls.

Familial heterogeneity of breast cancer risk was assessed among 4,159 first-degree female relatives of 1,074 population-based, young breast cancer cases (aged 20-54 years) diagnosed from December 1, 1980 to December 31, 1982 and 4,120 first-degree female relatives of 998 age- and race-matched, population-based controls from the metropolitan Detroit, Michigan, area. The family risk index method used for analysis considers family size, age, and race differences among families in the assessment of family risk. Families of cases showed a higher risk of breast cancer than did families of controls, with case families 1.80 to 4.24 times more likely to be defined as high risk than control families; the magnitude of the risk differential was dependent on the definition of high risk. Within the case families only, familial heterogeneity of risk was suggested, with a small proportion of families (less than 5%) at lower risk of breast cancer than most case families. A number of reproductive risk factors, age, race, and histologic type of cancer for the proband, and several family characteristics were investigated to help characterize the case families at higher and lower risk.     

Familial factors associated with malignant gliomas

Family histories of male patients with histologically confirmed malignant gliomas were compared to family histories of controls (wives). Included were 77 case families with 892 relatives and 77 control families with 719 relatives. Cases had significantly more siblings than controls (P = 0.02), although cases were not preferentially the oldest or the youngest sibs. Odds ratios of two or more were found for mental retardation, Parkinson's disease, and meningitis for the relatives of cases versus controls, but none were statistically significant. The excesses of Parkinson's disease and meningitis were explained by the family of one particularly interesting case containing three relatives with meningitis and two relatives with Parkinson's disease. Noteworthy age-adjusted odds ratios for cancer among relatives of cases compared to relatives of controls were 1.6 (95% confidence interval (CI) = 1.0-2.3) for cancer of any site, 2.4 (95% CI = 0.8-6.1) for breast cancer, and 4.0 (95% CI = 0.6-10.7) for lung cancer. Only the odds ratio for cancer of any site was statistically significant. Overall, 6 of 77 (8%) of cases came from families that included two or more relatives with breast or lung cancer in addition to the proband with malignant glioma. These three cancer sites may form familial clusters worthy of further evaluation in future studies by pedigree and genetic linkage analyses.     

418例肺癌患者家族癌症发病史流行病学调查分析

目的 了解肺癌患者中的家族癌症史的流行情况.方法 依据《人群疾病家族史和病史调查表》采用面对面的方式对巴中地区418例肺癌患者家族癌症史进行调查.结果 418例肺癌患者中家族史癌症阳性和肺癌阳性率分别为36.12％(151/418)和28.47％(119/418),两者间阳性率差异无统计学意义(P>0.05).患者家属...     

宣威肺癌的遗传因素初探

运用遗传流行病学的理论和方法，以肺癌病例的配偶做为对照，着重分析了肺癌家族史与宣威肺癌的关系。结果表明，肺癌家族史是肺癌的危险因素之一。既使调整了年龄、性别、吸烟、慢性肺疾患等因素的混杂作用，有肺癌家族史的人患肺癌的危险性仍然是没有肺癌家族史者患肺癌危险性的１．６０倍（Ｐ＜０．０５）。说明了遗传因素在宣威肺癌的发生过程中起着不可忽视的作用。